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1.
The learning capacities of rats with electrolytic lesions of the gustatory thalamus (GT) were investigated in 3 experiments. In Experiment 1, the presence of a taste cue failed to overshadow odor aversion learning in the lesioned rats, yet these same animals acquired normal taste and odor aversions. Thalamic lesions had no discernible effect on the acquisition of a conditioned flavor preference in Experiment 2. Finally, GT lesions completely reversed the anticipatory contrast effect shown by control subjects in Experiment 3. These results suggest that damage to the GT spares taste detection and recognition and simple associative learning but interferes with learning that involves more complex gustatory information processing. (PsycINFO Database Record (c) 2010 APA, all rights reserved)  相似文献   

2.
Neurologically intact rats expecting to receive a high-value reward (1.0 M sucrose), licked less for an unexpected low-value reward (0.15% saccharin) than did control subjects that only received the saccharin solution. This reward comparison effect, termed successive negative contrast, was eliminated after bilateral electrolytic lesions of the gustatory thalamus. The results are discussed in terms of disrupted memory processes that may have rendered the lesioned rats incapable of computing the relative reward value of the available solution (0. 15% saccharin) with respect to the memory of the preferred solution (1.0 M sucrose). (PsycINFO Database Record (c) 2010 APA, all rights reserved)  相似文献   

3.
In Exp I extensive hippocampal lesions retarded, but did not prohibit, the conditioning of a strong taste aversion to physiological saline (the CS) in 16 male Holtzman albino rats when illness (the UCS) was induced by apomorphine injection 15 min following ingestion of the saline. In Exp II hippocampal lesions reduced the aversiveness of novelty in a drinking fluid for 21 thirsty Ss. It is suggested that the mild impairment of taste aversion learning in Ss with hippocampal lesions was not the result of destruction of mnemonic mechanisms that serve to span the long CS-UCS interval but rather that the reduced intensity of the aversion resulted from a lesion-altered neophobic disposition that weakened the saliency of the novel flavor CS. (51 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)  相似文献   

4.
In Exp I, 24 intact male Lister rats were given either lactose or sucrose solutions. Although on 1st exposure they readily consumed lactose, its ingestion produced a conditioned taste avoidance (CTA) that was partly extinguished by repeated sucrose exposure after lactose conditioning. In Exp II, 8 Ss with large bilateral electrolytic lesions of the basolateral amygdala and 10 with either sham or no operations were given 2 pairings of saline with LiCl injections (upper gastrointestinal tract discomfort) and, in a separate condition, access to high levels of lactose (lower gastrointestinal tract discomfort). CTAs were measured both by 2-bottle tests and by video recordings of orofacial and somatic responses. The lesions attenuated LiCl-induced but not lactose-induced CTA, results demonstrating that a CTA can occur without the basolateral amygdala. Findings suggest that aversions based on distaste can be distinguished from avoidances based on danger, not only in terms of orofacial responses but also in terms of their neuroanatomical substrate. (31 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)  相似文献   

5.
Successive negative contrast is the exaggerated reduction of licking that occurs when rats expecting a high-value reward are given a low-value reward. This effect is typically investigated with a 24-hr retention interval between access periods. The present experiment tested the hypothesis that the absence of successive negative contrast in rats with bilateral lesions of the gustatory thalamus (GT) is due to a memory deficit. The results argue against this hypothesis by showing that, irrespective of retention-interval duration (7.5 min, 15 min, 45 min, 180 min, or 24 hr), lesioned rats failed to show successive negative contrast. As such, the data are consistent with the alternative view that GT lesions specifically disrupt the reward comparison mechanism that underlies successive negative contrast. (PsycINFO Database Record (c) 2010 APA, all rights reserved)  相似文献   

6.
Conditioned flavor aversions (CFA) are acquired by anesthetized rats but effects of various anesthetics on acquisition of aversions for separate odor and taste components are unknown. In Experiment 1, rats drank tomato juice and then were tranquilized with "Innovar-Vet" or "Rompun" before receiving injections of lithium chloride. Neither drug interfered with acquisition of aversions. Innovar-Vet alone produced no aversions; Rompun alone produced mild aversions but did not enhance aversions when combined with lithium. In Experiments 2 and 3, rats received a compound odor/taste cue as they drank and then were anesthetized with pentobarbital before lithium injections. Anesthesia alone produced negligible aversions but facilitated taste-lithium aversions. During odor tests, odor aversions were weaker than taste aversions. These data extend previous work and suggest that CFA does not result from ordinary classical conditioning. A tripartite notation that unites CFA and classical conditioning is discussed. (PsycINFO Database Record (c) 2010 APA, all rights reserved)  相似文献   

7.
Electrolytic lesions of the parabrachial nuclei (PBN) disrupt conditioned taste aversion (CTA) in the rat, but it is not known whether this effect is due to damaging axons of passage or to destruction of intrinsic neurons. We tested 10 rats with electrophysiologically guided, ibotenic acid lesions of the PBN (PBNx) to determine whether they could acquire an LiCl-induced CTA to l-alanine (0.3 M) or demonstrate a sodium appetite following furosemide treatment and overnight access to sodium deficient chow. Vehicle-treated and nonsurgical controls were included in the design. PBNx rats failed to develop a CTA, even after 3 conditioning trials. Moreover, more than 8 months later, a subset of the PBNx rats were again unable to learn a CTA using NaCl as the conditional stimulus (CS). After the furosemide treatment, the control rats drank an average of 20.3 ml of strong salt in 24 hr. The PBNx rats drank virtually no NaCl during the first 2 hr and averaged only 4.0 ml in 24 hr. In the PBN, damage to neuronal somata is more critical than interrupting fibers of passage for producing deficits in taste-guided behaviors. (PsycINFO Database Record (c) 2010 APA, all rights reserved)  相似文献   

8.
A new hypothesis (and supporting data) provides a solution to the 25-yr-old paradox whereby positively reinforcing drugs of abuse also support a conditioned taste aversion (CTA). The results show that unlike LiCl-induced CTAs, morphine- and cocaine-induced suppression of conditioned stimulus (CS) intake depends on the rewarding properties of the gustatory CS. This finding argues against the long-standing CTA interpretation in favor of a new reward comparison account. That is, rats decrease intake of a gustatory CS following taste–drug pairings because the value of the CS is outweighed by that of a highly reinforcing psychoactive drug. Suppression of CS intake, then, is a consequence of the well-documented positive reinforcing, rather than the hypothetical aversive, properties of drugs of abuse. (PsycINFO Database Record (c) 2010 APA, all rights reserved)  相似文献   

9.
Rats with bilateral, electrophysiologically guided, ibotenic acid lesions of the gustatory thalamus (THLX) were tested for their ability to perform a variety of taste-guided behaviors. First, in daily 30-min sessions, the rats were given repeated 10-s access periods to a range of concentrations of sucrose, NaCl, or QHCl, plus water. Both the control and the THLX rats exhibited similar concentration-response functions, regardless of hydrational state. Next, on 3 trials, the rats were given 15 min access to 0.3 M l-alanine and then injected with LiCl (0.15 M, 1.33 ml/100 g body weight ip). All rats learned a taste aversion following 1 pairing with LiCl. Finally, on 3 separate occasions, the rats were injected with furosemide, and Na(+)-appetite was evaluated 24 hr later. All rats expressed an equivalent sodium appetite after the first furosemide injection, but only the control rats increased intake of 0.51 M NaCl with repeated sodium depletions. These observations reinforce prior data implying that an intact gustatory thalamus is not necessary for the expression of some taste-guided behaviors.  相似文献   

10.
Reports results of 8 experiments with a total of 327 male Sprague-Dawley rats. Lesions to the basolateral amygdala produced permanent impairment in Ss' ability to learn a taste aversion. When lesions were administered after Ss had already learned an aversion, there was complete loss of the aversion. Ss with amygdala lesions also had a diminished neophobic response when presented with a novel solution and showed a more generalized aversion to water after a sucrose-sickness trial. Whether a solution was novel or familiar affected the learning of an aversion for controls more than it did for Ss with amygdala lesions. Ss with amygdala damage also showed less sodium appetite than normals in response to desoxycorticosterone acetate injections. These results indicate that rats with amygdala lesions have deficits in recognizing the significance of stimuli. (49 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)  相似文献   

11.
The hedonic properties of delta-9-tetrahydrocannabinol (THC) were assessed in place and taste conditioning paradigms in both Lewis and Sprague-Dawley rat strains. THC produced place avoidance, taste avoidance, and aversive taste reactivity responses in both strains. The Lewis strain displayed more aversive taste reactions and a stronger taste avoidance when conditioned with lower doses of THC than did the Sprague-Dawley strain of rats. THC is an anomalous drug of abuse that appears to be aversive to rats when assessed by these measures. (PsycINFO Database Record (c) 2010 APA, all rights reserved)  相似文献   

12.
Trained 50 male Sprague-Dawley rats in a saccharin-anise discriminated taste aversion paradigm. Saline or pentylenetetrazol (metrazol), an amnesia agent, was administered either within or after the CS-UCS interval. Retrograde amnesia (RA) resulted in both cases, but was stronger when induced after the UCS. Due to the nature of the discriminated-avoidance paradigm used, the RA could not be explained in terms of the punishing effects of the RA treatment or general disinhibition. Data indicate that an amnesic treatment causes a memory deficit, at least part of which is due to the disruption of the CS trace. (20 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)  相似文献   

13.
14.
Results from 3 experiments indicate that severing the subdiaphragmatic vagus in male Sprague-Dawley rats increased the rate of extinction of learned taste aversions. In Exp I, when the illness-inducing agent was the blood-borne toxin apomorphine, vagotomized Ss tended to consume more saccharin than controls during repeated extinction tests. In Exp II, vagotomy disrupted retention and increased extinction of a preoperatively acquired saccharin aversion. Disruptions were found when the taste aversion was induced by copper sulfate, a local gastric irritant, or apomorphine. Exp III demonstrated that vagotomy did not affect retention or extinction of a shock-induced conditioned emotional response to noise. It is concluded that integrity of the vagus is not necessary for acquisition of a learned taste aversion when a blood-borne toxin is used as the illness-inducing agent. However, the vagus apparently mediates an integral portion of the CR following taste–illness acquisition. (24 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)  相似文献   

15.
372 golden hamsters and 120 Sprague-Dawley rats tasted 1 of 27 solutions before receiving an ip injection of apomorphine, then were tested for aversions to 4 solutions prototypic of human taste qualities: sucrose, NaCl, HCl, and quinine HCl. With most of the solutions described as sweet employed as CSs, Ss acquired an aversion to sucrose. With CSs described as either salty or sour by humans, Ss acquired an NaCl aversion in the former case or an HCl aversion in the latter case; an aversion to quinine HCl was acquired with 2 of the 3 CSs described as sour. With most of the CSs described as bitter or as having a bitter component, Ss acquired a quinine HCl aversion. Patterns of S activity evoked across 4 classes of peripheral gustatory neurons when the CSs were applied to the tongue were similar to the patterns of aversions across the 4 test stimuli for the CSs. This suggests that 4 neural channels mediate the sensations evoked by the 4 test solutions in rats and hamsters, perhaps even in human beings. (26 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)  相似文献   

16.
Tested the proposal that learned safety accounts for the delay gradient in learned taste aversions in 4 experiments. In Exp I and II, 132 female Sprague-Dawley rats drank a small quantity of a nontoxic solution toward which they had a mild aversion. It was found, in support of the learned safety concept, that the intake in a 2nd test was a function of the delay time between tests. Exp III with 72 Ss demonstrated that no additional curve of learned safety would occur when Ss had previously received extensive experience with the solution. Exp IV with 81 Ss found, however, that learned safety was not a sufficient explanation for the delay gradient in learned taste aversions by showing that the gradient still persisted even when the experimental procedure minimized the effects of learned safety. (PsycINFO Database Record (c) 2010 APA, all rights reserved)  相似文献   

17.
The experiments presented in this article were designed to examine whether area postrema (AP) lesions attenuate LiCl-induced conditioned taste aversions (CTAs) by disruption of information about the illness-producing properties of LiCl or by a lesion-induced malaise. Reversible lesioning of the AP caused by cooling induced a CTA in male rats. The cooling-induced CTA could be blocked if males were exposed to cooling for several days before acquisition day. Acquisition of a LiCl-induced CTA was blocked in males if they were exposed to cooling before acquisition day and during LiCl administration on acquisition day was attenuated but not blocked in males if they were exposed to cooling only before acquisition day, and was unchanged in males if they were exposed to cooling only during LiCl administration. Taken together these results indicate that the AP is important for acquisition of LiCl-induced CTAs but that inactivation of this area is so aversive it will induce CTAs that can obscure the attenuation of LiCl-induced aversions.  相似文献   

18.
In 5 experiments, administration of lithium chloride, copper sulfate, and apomorphine to male Sprague-Dawley rats each stimulated the secretion of oxytocin (OT) and, to a much lesser degree, arginine vasopressin. These agents are assumed to cause visceral illness in rats because of their effectiveness in promoting the acquisition of learned taste aversions (LTAs). CuSO?, but not LiCl, had a greater effect on plasma OT levels when administered intraperitoneally rather than intravenously. Results suggest that LiCl stimulates OT secretion by central chemoreceptor activation, whereas CuSO? acts predominantly by local peritoneal irritation. A causal role for circulating OT in the acquisition of LTAs was not found. Peripheral levels of OT may represent a quantifiable marker of visceral illness in rats and therefore might be useful in the interpretation of behavioral studies in which CTAs are produced, provided that other stimuli of neurohypophyseal secretion are absent. (34 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)  相似文献   

19.
Rats with either electrolytic (Experiment 1) or excitotoxic lesions (Experiment 2) that had been electrophysiologically centered in the gustatory zone of the parabrachial nuclei (PBN) were tested for sucrose and NaCl taste detection thresholds in a conditioned avoidance task. With 1 exception, all of these rats had previously shown severe deficits in acquiring an LiCl-based conditioned taste aversion (CTA) to sucrose, NaCl, or alanine. The rats with excitotoxic lesions also had failed to express a depletion-induced sodium appetite. Despite the uniformity of these deficits, the rats with lesions exhibited varied performance in the detectability task. Roughly ? of the rats did not perform competently, ? had elevated thresholds, and ? showed no or only marginal impairments in taste detectability. These findings demonstrate that the elimination of CTA following PBN lesions is not necessarily linked to an impairment in taste signal detection. Thus, PBN-induced deficits on 1 taste-related task do not entirely correspond with impairments on another. (PsycINFO Database Record (c) 2010 APA, all rights reserved)  相似文献   

20.
This study examined the effects of electrophysiologically placed electrolytic lesions in the gustatory zone of the parabrachial nuclei (PBN) on the rat's taste-guided unconditioned licking of quinine hydrochloride during repeated 10-sec trials. Concentration–response functions measured in water-deprived rats before and after surgery significantly shifted to the right as a result of the bilaterally placed lesions. These same rats were tested on their ability to acquire a lithium chloride (LiCl)-based conditioned taste aversion (CTA) to 0.1 M sucrose. Although the largest lesions severely affected performance in both tasks, there was only a modest correlation (r?=?–.447) between the extent of the lesion-induced shift in the quinine concentration–response curves and the degree of sucrose intake suppression after the first CTA conditioning trial. Thus, PBN lesions can disrupt performance on both tasks, but it appears that the neural processes governing unconditioned responsiveness to quinine may be to some extent dissociable from those subserving acquisition of a sucrose–LiCl-based CTA. (PsycINFO Database Record (c) 2010 APA, all rights reserved)  相似文献   

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